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The Journal of Immunology, 2004, 173: 3748-3754.
Copyright © 2004 by The American Association of Immunologists

Murine Plasmacytoid Dendritic Cells Initiate the Immunosuppressive Pathway of Tryptophan Catabolism in Response to CD200 Receptor Engagement1

Francesca Fallarino*, Carine Asselin-Paturel{dagger}, Carmine Vacca*, Roberta Bianchi*, Stefania Gizzi*, Maria Cristina Fioretti*, Giorgio Trinchieri{dagger}, Ursula Grohmann* and Paolo Puccetti2,*

* Department of Experimental Medicine, University of Perugia, Perugia, Italy; and {dagger} Laboratory for Immunological Research, Schering-Plough Research Institute, Dardilly, France

In this study, using a soluble CD200-Ig fusion protein, we provide evidence that murine dendritic cells (DCs) possess a functional CD200R, whose engagement results in the reinforcement or appearance of immunosuppressive properties in these cells. In particular, the plasmacytoid subset (CD11c+B220+120G8+) of splenic DCs (pDCs) is induced by CD200-Ig to express the enzyme IDO, which initiates the tolerogenic pathway of tryptophan catabolism. As a result, pDCs are capable of suppressing Ag-specific responses in vivo when transferred into recipient hosts after treatment with CD200-Ig. IDO induction in pDCs through CD200R engagement requires type I IFNR signaling. Although the release of IFN-{alpha} may contribute to the full expression of CD200-Ig activity, autocrine IFN-{alpha} is unlikely to mediate alone the effects of CD200R engagement. These data prospect novel functions for both pDCs and the CD200-CD200R pair in the mouse. At the same time, these data underscore the possible unifying role of the IDO mechanism in immune tolerance.


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